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The effect of LCD on suppressing inflammation in CCl 4 ‐induced mice. (A) The levels of serum IL‐1β were measured. (B) The concentrations of <t>serum</t> <t>IL‐6</t> were evaluated. (C) The serum TNF‐α levels were determined. (D) Serum IL‐10 was analysed. (E) The IL‐1β/IL‐10 ratio was calculated. (F) The IL‐6/IL‐10 ratio was derived. (G) The TNF‐α/IL‐10 ratio was established.
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Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, <t>and</t> <t>IL-13</t> levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.
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Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, <t>and</t> <t>IL-13</t> levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.
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Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, <t>and</t> <t>IL-13</t> levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.
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iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression <t>(IL-6,</t> TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.
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Suppression of proinflammatory cytokine production and M1-type macrophage polarization by a supersulfide donor in livers from APAP-treated mice. (A–C) Levels of IL-1β, <t>IL-6,</t> and IL-10 in liver tissue. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous NAC-S2 administration at 30 min and 2 h post-APAP. Livers were harvested 24 h after APAP administration, and cytokine levels were quantified by ELISA. (D) Western blot analysis of hepatic iNOS and Arg-1 expression. (E, F) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.
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Immunomodulatory effects of the bioengineered LEVs Tet−PKM2 @TA in terms of their ability to modulate macrophage polarization in vitro . The macrophages were treated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) The relative mRNA expression levels of M1 polarization-related genes <t>(</t> <t>IL-6</t> and IL-1β ) and M2 polarization-related genes ( IL-4 and Arg-1 ) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (qRT‒PCR) ( n = 3). ( B ) Concentrations of M1-related cytokines (IL-6 and TNF-α) and M2-related cytokines (IL-4 and IL-10) in the supernatants of the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (ELISA) ( n = 3). ( C ) Representative immunofluorescence images and quantification of the expression levels of M1-related proteins (iNOS and CCR7) and M2-related proteins (CD163, CD206, and Arg-1) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( A , B , and C ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
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Immunomodulatory effects of the bioengineered LEVs Tet−PKM2 @TA in terms of their ability to modulate macrophage polarization in vitro . The macrophages were treated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) The relative mRNA expression levels of M1 polarization-related genes <t>(</t> <t>IL-6</t> and IL-1β ) and M2 polarization-related genes ( IL-4 and Arg-1 ) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (qRT‒PCR) ( n = 3). ( B ) Concentrations of M1-related cytokines (IL-6 and TNF-α) and M2-related cytokines (IL-4 and IL-10) in the supernatants of the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (ELISA) ( n = 3). ( C ) Representative immunofluorescence images and quantification of the expression levels of M1-related proteins (iNOS and CCR7) and M2-related proteins (CD163, CD206, and Arg-1) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( A , B , and C ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.
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Image Search Results


The effect of LCD on suppressing inflammation in CCl 4 ‐induced mice. (A) The levels of serum IL‐1β were measured. (B) The concentrations of serum IL‐6 were evaluated. (C) The serum TNF‐α levels were determined. (D) Serum IL‐10 was analysed. (E) The IL‐1β/IL‐10 ratio was calculated. (F) The IL‐6/IL‐10 ratio was derived. (G) The TNF‐α/IL‐10 ratio was established.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Longchai Decoction Treated the Fibrosis of Liver Induced by CCl 4 Regulates Nrf2/ GPX4 Pathway to Suppress Ferroptosis

doi: 10.1111/jcmm.71151

Figure Lengend Snippet: The effect of LCD on suppressing inflammation in CCl 4 ‐induced mice. (A) The levels of serum IL‐1β were measured. (B) The concentrations of serum IL‐6 were evaluated. (C) The serum TNF‐α levels were determined. (D) Serum IL‐10 was analysed. (E) The IL‐1β/IL‐10 ratio was calculated. (F) The IL‐6/IL‐10 ratio was derived. (G) The TNF‐α/IL‐10 ratio was established.

Article Snippet: Mouse interleukin‐1β (IL‐1β, EK201B), IL‐6 (EK206), and TNF‐α (EK282) were bought from Lianke Bioengineering Institute (Shanghai, China).

Techniques: Derivative Assay

Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.

Journal: Redox Biology

Article Title: Nrf2 pathway mediates copper oxide nanoparticle-induced exacerbation of allergic asthma

doi: 10.1016/j.redox.2026.104180

Figure Lengend Snippet: Effects of CuONPs on allergic inflammation and oxidative stress in OVA-induced asthmatic mice. (A) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (B–F) Total and differential inflammatory cell counts in BALF. (G–L) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (M and N) Total IgE and OVA specific IgE levels in serum. (O and P) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 6 mice/group). ∗∗ p < 0.01 and ∗∗∗ p < 0.001 versus NC group. # p < 0.05, ## p < 0.01, and ### p < 0.001 versus OVA group.

Article Snippet: BALF was centrifuged at 300× g for 10 min at 4 °C, and the supernatant was stored for cytokine analysis using commercially available enzyme-linked immunosorbent assay (ELISA) kits to quantify IL-1β, IL-6, tumor necrosis factor (TNF)-α, IL-4, IL-5, and IL-13 (R&D Systems, Minneapolis, MN, USA; Cat. No. MLB00C, M6000B, MTA00B, M4000B, M5000, and M1300CB, respectively).

Techniques: Enzyme-linked Immunosorbent Assay, Activity Assay

Effects of Nrf2 overexpression on allergic inflammation and oxidative stress in CuONP-exposed asthmatic mice. (A) Immunofluorescence analysis of lung tissue from mice administered PBS or AAV2/8-GFP via intratracheal instillation. (B) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (C–G) Total and differential inflammatory cell counts in BALF. (H–M) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (N and O) Total IgE and OVA specific IgE levels in serum. (P and Q) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 3 mice/group for panels A; n = 6 mice/group for panels B–Q). In panel B, ## p < 0.01 indicates significant differences between GFP-NC and GFP-OVA, and ∗∗ p < 0.01 indicates significant differences between GFP-OVA + CuONPs and Nrf2-OVA + CuONPs. For panels C–Q, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between AAV-GFP and AAV-Nrf2 within each condition.

Journal: Redox Biology

Article Title: Nrf2 pathway mediates copper oxide nanoparticle-induced exacerbation of allergic asthma

doi: 10.1016/j.redox.2026.104180

Figure Lengend Snippet: Effects of Nrf2 overexpression on allergic inflammation and oxidative stress in CuONP-exposed asthmatic mice. (A) Immunofluorescence analysis of lung tissue from mice administered PBS or AAV2/8-GFP via intratracheal instillation. (B) Airway hyperresponsiveness assessed as total respiratory system resistance in response to methacholine challenge (10, 20, and 40 mg/mL). (C–G) Total and differential inflammatory cell counts in BALF. (H–M) IL-1β, IL-6, TNF-α, IL-4, IL-5, and IL-13 levels in BALF, measured by ELISA. (N and O) Total IgE and OVA specific IgE levels in serum. (P and Q) MDA levels and SOD activity in lung tissue. Data are presented as means ± SD (n = 3 mice/group for panels A; n = 6 mice/group for panels B–Q). In panel B, ## p < 0.01 indicates significant differences between GFP-NC and GFP-OVA, and ∗∗ p < 0.01 indicates significant differences between GFP-OVA + CuONPs and Nrf2-OVA + CuONPs. For panels C–Q, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between AAV-GFP and AAV-Nrf2 within each condition.

Article Snippet: BALF was centrifuged at 300× g for 10 min at 4 °C, and the supernatant was stored for cytokine analysis using commercially available enzyme-linked immunosorbent assay (ELISA) kits to quantify IL-1β, IL-6, tumor necrosis factor (TNF)-α, IL-4, IL-5, and IL-13 (R&D Systems, Minneapolis, MN, USA; Cat. No. MLB00C, M6000B, MTA00B, M4000B, M5000, and M1300CB, respectively).

Techniques: Over Expression, Immunofluorescence, Enzyme-linked Immunosorbent Assay, Activity Assay

iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: Recombinant MDK protein triggers the activation of inflammatory cytokines through the NF-κB signaling pathway. (A, B) IL-6, TNFα, and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were treated with recombinant MDK protein (600 ng/mL). Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (C, D) Western blotting analysis of NF-κB signaling pathway molecules in MC3T3-E1 cells treated with recombinant MDK protein for 7 days during osteoblastic differentiation. Inter-group comparisons were analyzed by two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (E, F) IL-6 and IL-1β expression levels were detected using Western blotting. MC3T3-E1 cells were pretreated with 10 μM BAY 11–7082. Osteogenic differentiation was induced for 7 days. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05 and ∗∗ p < 0.01.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Recombinant, Activation Assay, Expressing, Western Blot, Two Tailed Test

Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Recombinant

Suppression of proinflammatory cytokine production and M1-type macrophage polarization by a supersulfide donor in livers from APAP-treated mice. (A–C) Levels of IL-1β, IL-6, and IL-10 in liver tissue. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous NAC-S2 administration at 30 min and 2 h post-APAP. Livers were harvested 24 h after APAP administration, and cytokine levels were quantified by ELISA. (D) Western blot analysis of hepatic iNOS and Arg-1 expression. (E, F) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Suppression of proinflammatory cytokine production and M1-type macrophage polarization by a supersulfide donor in livers from APAP-treated mice. (A–C) Levels of IL-1β, IL-6, and IL-10 in liver tissue. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous NAC-S2 administration at 30 min and 2 h post-APAP. Livers were harvested 24 h after APAP administration, and cytokine levels were quantified by ELISA. (D) Western blot analysis of hepatic iNOS and Arg-1 expression. (E, F) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Control

Effects of NAC-S2, oxNAC, and NAC on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous administration of sulfur compounds (NAC-S2, oxNAC, or NAC) at 30 min and 2 h post-APAP. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D) Quantification of necrotic area in liver. Macroscopic appearance and H&E staining of liver tissues are shown in Hepatic cytokine levels: IL-1β (E), IL-6 (F), and IL-10 (G). (H) Western blot analysis of iNOS and Arg-1 expression in liver. (I, J) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Effects of NAC-S2, oxNAC, and NAC on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous administration of sulfur compounds (NAC-S2, oxNAC, or NAC) at 30 min and 2 h post-APAP. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D) Quantification of necrotic area in liver. Macroscopic appearance and H&E staining of liver tissues are shown in Hepatic cytokine levels: IL-1β (E), IL-6 (F), and IL-10 (G). (H) Western blot analysis of iNOS and Arg-1 expression in liver. (I, J) Quantification of Western blot band intensities. Relative protein levels were normalized to β-actin. Uncropped blots are shown in . Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 3). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Staining, Western Blot, Expressing, Control

Effects of the supersulfide donor TGS4 on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous injection of TGS4 at 30 min and 2 h post-APAP. Two different doses were used as indicated. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D–F) Hepatic cytokine levels: IL-1β (D), IL-6 (E), and IL-10 (F). Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 4). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Journal: Redox Biology

Article Title: Hepatic supersulfides attenuate acetaminophen-induced liver injury via enhanced detoxification and anti-inflammatory mechanisms

doi: 10.1016/j.redox.2026.104140

Figure Lengend Snippet: Effects of the supersulfide donor TGS4 on APAP-induced liver injury. (A) Experimental protocol. Mice were intraperitoneally administered APAP (330 mg/kg), followed by subcutaneous injection of TGS4 at 30 min and 2 h post-APAP. Two different doses were used as indicated. Blood was collected at 8, 12, and 24 h post-APAP, and liver tissue was harvested at 24 h post-APAP. (B, C) Time-course of serum ALT and AST levels. (D–F) Hepatic cytokine levels: IL-1β (D), IL-6 (E), and IL-10 (F). Statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc multiple comparisons test. Data were expressed as means ± SD (n ≥ 4). ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001; # P < 0.05, # # P < 0.01, # # # P < 0.001 compared to control group.

Article Snippet: Mouse IL-1β/IL-1F2 Quantikine ELISA Kit (MLB00C), Mouse IL-6 Quantikine ELISA Kit (M6000B-1), and Mouse IL-10 Quantikine ELISA Kit (M1000B) were obtained from R&D Systems (Minneapolis, MB, USA).

Techniques: Injection, Control

Immunomodulatory effects of the bioengineered LEVs Tet−PKM2 @TA in terms of their ability to modulate macrophage polarization in vitro . The macrophages were treated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) The relative mRNA expression levels of M1 polarization-related genes ( IL-6 and IL-1β ) and M2 polarization-related genes ( IL-4 and Arg-1 ) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (qRT‒PCR) ( n = 3). ( B ) Concentrations of M1-related cytokines (IL-6 and TNF-α) and M2-related cytokines (IL-4 and IL-10) in the supernatants of the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (ELISA) ( n = 3). ( C ) Representative immunofluorescence images and quantification of the expression levels of M1-related proteins (iNOS and CCR7) and M2-related proteins (CD163, CD206, and Arg-1) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( A , B , and C ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Immunomodulatory effects of the bioengineered LEVs Tet−PKM2 @TA in terms of their ability to modulate macrophage polarization in vitro . The macrophages were treated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) The relative mRNA expression levels of M1 polarization-related genes ( IL-6 and IL-1β ) and M2 polarization-related genes ( IL-4 and Arg-1 ) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (qRT‒PCR) ( n = 3). ( B ) Concentrations of M1-related cytokines (IL-6 and TNF-α) and M2-related cytokines (IL-4 and IL-10) in the supernatants of the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (ELISA) ( n = 3). ( C ) Representative immunofluorescence images and quantification of the expression levels of M1-related proteins (iNOS and CCR7) and M2-related proteins (CD163, CD206, and Arg-1) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( A , B , and C ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Article Snippet: Kits were sourced as follows: TNF-α, IL-4, and IL-10 from Fankew (Shanghai Kexing Trading Co., Ltd., China) and IL-6 from Proteintech.

Techniques: In Vitro, Control, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence